INTRODUCTION
Necrotizing fasciitis is a progressive,
generally rapidly spreading, inflammatory
pro-cess located in the deep fascia with secondary
necrosis of subcutaneous tissues and skin.
The speed of skin involvement is directly
related and proportional to the thickness
of the subcutaneous layer. This necrosis manifests
itself as an extensive undermining of the
skin and subcutis. As a rule, the patient
is seriously ill, septic with a high fever.
Current recommendations for the treatment
of necrotizing fasciitis in human patients
include aggressive surgical debridement, broad-spectrum
multiple antibiotic therapy and adjunctive
hyperbaric oxygen. Hyperbaric oxygen (HBO)
therapy is defined as therapy in which the
patient breathes 100% oxygen at a pressure
greater than that at sea level, that is, greater
than one atmosphere absolute (ATA).
CLINICAL REPORT
An approximately 8-month-old female kitten
was admitted to the hospital with an apparent
traumatic hernia of the left abdominal wall.
She was also pregnant. Two students found
her in the parking lot of their apartment
complex. They reported that she had been
seen in the area for a few weeks and appeared
normal the day before. That same afternoon,
she was taken to surgery. At laparotomy,
an OVH was performed on a large gravid uterus.
A 2 cm tear in the dorsolateral abdominal
wall was found with duodenum and greater
omentum in the SQ space. A 1 cm tear in
the duodenum was apparent. Ingesta contaminated
the SQ space and the abdomen. After repair
and closure of the abdomen, the SQ site
was lavaged with the Betadine and a penrose
drain placed. The kitten was unexpectedly
painful the first two days post-operatively,
but improved on SQ fluids and Cefazolin.
By day 3, she was eating and grooming. Six
days post-op a necrotic area became apparent
near the site of the hernia. A 20cm by 10cm
area of se-vere skin, fat and muscle necrosis
was extensively debrided, flushed and bandaged.
Closure was impossible because of the size
of the defect and the degree of infection.
For pain associated with the wounds and
bandage changes, a 25ug Fentanyl patch was
employed. Enrofloxacin and Cefazolin were
given every 12 hours. Bandage changes occurred
daily. The wound was lavaged with Betadine
or Chlorhexiderm at each bandage change.
A topical cephalosporin was applied during
bandage changes. A second debridement was
performed 3 days later. At that time, the
margins of the wound extended from the scapula
distally to the inguinal region and from
the dorsum ventrally beyond the midline
to the other side of the abdomen, approx.
23 by 20 cm. (Figure 1) This extent of this
wound was about 40% of the trunk or axial
area. She was not expected to survive. On
the tenth day of hospitalization, hyperbaric
therapy began." All other treatments
were continued as described. She was placed
in a small plexi-glass induction chamber
commonly used in veterinary medicine with
inflow and outflow connections. (Figure
2) Each session, called a "dive",
lasted over one hour and took place at 2.36
atmospheres within the diving chamber. 100%
oxygen was delivered into the chamber and
expired air passively evacuated from the
chamber. After 2 dives, a granulation bed
began to form. Evidence of purulence dramatically
diminished. Emphysema appeared in both back
legs due to air leakage from the caudal
ingui-nal margin of the defect. Both back
legs were wrapped in a cruciate pattern
integrated with the abdominal wrap. All
other therapy contin-ued. The emphysema
in her legs resolved as wound contracture
proceeded and adhesion of the skin and SQ
to the body wall began. . Healing continued
rapidly. After eight days, the wound bed
appeared increasingly vascular and became
more painful as nerve endings surfaced.
The ventral margins of the wound began to
bleed during bandage placement. After 2
weeks, the wound bed had contracted to 9
by 10 cm, approx. 1/5 the original size.
After four weeks of hyperbaric sessions,
the dorsal margins of the wound were apposed.
Ventrally the wound measured 8 by 2 cm.
(Figure 3) Bandaging was discontinued after
one month. In all, she dove in 32 separate
ses-sions for a total of 2430 minutes. A
scar appeared at the most central aspect
of the wound where the two wound margins
apposed. It is a thin line that travels
from the dorsal lumbar area beyond the mid-line.
It is approx. 5 mm wide at its widest point
and is the only part of her body where far
re-growth has not occurred.
Discussion
It is highly characteristic of necrotizing
fasci-it is that the spread of the fascial
necrosis is more extensive than the visible
changes of the skin. The apparently normal
skin and subcuta-neous tissue are loosened
from the underlying necrotic fascia over
a great distance from the original wound.
Skin necrosis is secondary to thrombosis
of subcutaneous blood vessels. In this case,
the subcutaneous layer was thin and the
skin became involved within 5 days. The
kitten was extremely painful, became less
so and then very painful during the first
weeks of hyperbaric therapy. Hyperbaric
oxygen therapy can be ad-ministered in an
individual pressurized deliv-ery chamber
or in a multi-position chamber. In this
case, a chamber large enough to accomo-date
at least six humans was used. Treatment
regimens vary according to the disorder.
De-livery of 100% oxygen at 2.0 to 2.4 ATA
is standard for adult human patients. 2
Oxygen was delivered at 2.36 ATA, usually
for 50 minutes with 15 minute com-pression
(before) and decompression (after) phases.
Breathing oxygen at this pressure in-creases
oxygen tension in the capillaries that surround
ischemic tissue and promotes oxy-gen diffusion
from the capillaries to the tissue. Hyperbaric
oxygen provides a signifi-cant increase
in tissue oxygenation in the hy-poperfused,
infected wound. This elevation in oxygen
tension induces powerful positive changes
in the wound repair process. HBO directly
enhances fibroblastic replication, col-lagen
synthesis and the process of neovascu-larization
in ischemic tissue. By providing mo-lecular
oxygen at the cellular level it also in-creases
leukocyte bactericidal activity. The hyperoxic
conditions increase the production of intracellular
and extracellular oxygen-derived free radicals
in leukocytes and phagocytes, enhancing
the bacteriocidal ef-fects on strict anaerobic
organisms and some microaerobic organisms.
This can be roughly summarized as stimula-tion
of the host defense and repair mecha-nisms.
Hyperbaric oxygen therapy is a useful technique
in the management of problem wounds in which
hypoxia and/or infection are the underlying
etiologic factors.
References:
Bakker, Jan Dirk, SelectedAerobic and Anaerobic
Soft Tissue Infections, Diagnosis and the
Use of Hy-perbaric Oxygen as an Adjunct,
in Hyperbaric Medi-cine Practice, p. 396-417.
Hosgood, Elkins and Hill, "Hyperbaric
Oxygen Ther-apy: Mechanism and Potential
Applications", The Compendium of Continuing
Education, Vol. 12 No. 11, 1990, p. 1589-1593
Inquiries about therapy may be made to the
author or:
Western Hyperbaric, L.L.C.
Mr. Mitch Hoggard, President
3880 Morrow Ln., Suite 4
Chico Ca. (530) 894-3288
Matos and Nunez, Enhancement of Healing
in Se-lected Problem Wounds, in Hyperbaric
Medicine Practice, p. 590-611.
ABOUT THE AUTHOR:
Elizabeth Colleran is a 1990 graduate of
Tufts University School of Veterinary Medicine.
She completed a one year in-ternship at
Southshore Veterinary Asso-ciates before
moving to California. In 1996, she was awarded
a Master of Sci-ence degree in Animals and
Public Policy from Tufts University School
of Veteri-nary Medicine. She owns Chico
Hospital for Cats, an AAHA hospital in Chico.
|